Characterization of Hippocampal Sclerosis in Individuals With Calcified Neurocysticercosis ABSTRACT Most of the global burden of epilepsy occurs in poor regions of the world, reflecting increased prevalence of risk factors such as perinatal brain damage, traumatic brain injury, and infections of the nervous system including neurocysticercosis (NCC). NCC is endemic in most developing countries, and the prevalence of seizures and epilepsy is consistently increased in individuals with NCC when compared to the general population. Epilepsy is more prevalent in cysticercosis-endemic regions, and cases of chronic focal seizures semiologically related to the localization of a parasitic lesion are frequent. Perhaps more interestingly, information from patients with refractory epilepsy and NCC suggests that in some patients parasites might be involved in epileptogenesis by inducing hippocampal damage, which can become the site of seizure onset. We propose to take advantage of an existing cohort of 228 patients with calcified cerebral cysticercosis lesions as well as 50 control patients with spinal pathologies without cerebral involvement, to demonstrate the association between NCC and hippocampal sclerosis, and to characterize the clinical, neurophysiological, and neuroimaging characteristics associated with hippocampal sclerosis in these individuals. Participants will have hippocampal assessment by non-contrasted brain MRI, and computational morphometry analysis of MRI will be used to characterize specific neocortical and subcortical patterns of atrophy (with the use of volumetric MRI and cortical thickness measures) and to determine whether HS in these patients has the specific pattern of CA2 sparing found in mesial temporal lobe epilepsy or another, non-specific pattern. EEG and Video EEG will be performed to determine whether the location of the epileptogenic region correlates with the location of the HS or a calcified lesion elsewhere. The frequencies of all factors potentially associated with HS (including but not restricted to time with seizures, cumulative number of previous seizures, type of seizures, number and localization of brain calcifications, and EEG abnormalities) will be compared between individuals with and without HS. If NCC-associated HS is the epileptogenic region, and is similar to the HS in MTLE it would provide an opportunity to study epileptogenesis clinically for the most common form of intractable epilepsy.